Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay has been developed that permits reliable measurements of plasma arginine vasopressin (AVP) at concentrations as low as 0.5 pg/ml in sample volumes of 1 ml or less. Nonhormonal immunoreactivity associated with the plasma proteins is eliminated by acetone precipitation before assay, leaving unaltered a component that is immunologically and chromatographically indistinguishable from standard AVP. Storage of plasma results in a decline in AVP concentration and, thus, must be carefully regulated. The plasma AVP values obtained by our method approximate the anticipated levels and vary in accordance with physiologic expections. In recumbent normal subjects, plasma AVP ranged from (mean +/-SD) 5.4+/-3.4 pg/ml after fluid deprivation to 1.4+/-0.8 pg/ml after water loading, and correlated significantly with both plasma osmolality (r=0.52; P<0.001) and urine osmolality (r=0.77; P<0.001). After fluid restriction, plasma AVP was uniformly normal relative to plasma osmolality in patients with nephrogenic diabetes insipidus and primary polydipsia but was distinctly subnormal in all patients with pituitary diabetes insipidus. The infusion of physiologic amounts of posterior pituitary extract caused a dose-related rise in plasma vasopressin that afterwards declined at the expected rate (t(1/2)=22.5+/-4 min). We conclude that, when used appropriately, our radioimmunoassay method provides a useful way of assessing AVP function in man.
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PMID:Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma. 472 63

A 5-year-old, domestic long-haired cat was presented for examination because of polydipsia, polyuria and inappropriate urination of 3 months' duration. Neurogenic diabetes insipidus was diagnosed, based on hyposthenuria with failure to concentrate urine in response to water deprivation and positive response to antidiuretic hormone administration. Treatment with hydrochlorothiazide or chlorpropamide orally gave inadequate antidiuresis, but response to injections of vasopressin tannate in oil was sufficient for satisfactory management.
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PMID:Idiopathic neurogenic diabetes insipidus in a cat. 663 29

Central diabetes insipidus (DI) patients showed impairments in short- and long-term memory functions, but not in attention and concentration, as compared to healthy individuals. A single i.m. injection or sub-chronic intranasal administration of either lysine-vasopressin (LVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) normalized the disturbed memory functions in DI patients. These peptides also improved memory functions in healthy individuals.
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PMID:Effects of lysine-vasopressin and 1-deamino-8-D-arginine-vasopressin on memory in healthy individuals and diabetes insipidus patients. 717 72

Central diabetes insipidus was diagnosed by vasopressin measurements during hypertonic stimulation in a 9-year-old male giant Schnauzer with polyuria and polydipsia. The impaired release of vasopressin was believed to be caused by a large pituitary tumor, which was visualized by computed tomography. Studies of the function of the anterior lobe and the pars intermedia of the pituitary gland were conducted, and high concentrations of ACTH and alpha-melanotrophic hormone (alpha-MSH) were found without concomitant hyperadrenocorticism. Studies of the molecular size of the immunoreactive ACTH in plasma by gel filtration revealed that most of the circulating immunoreactivity was not ACTH but its precursor pro-opiomelanocortin (POMC) and low-molecular-weight POMC-derived peptides. The pituitary tumor of this dog probably originated from melanotrophic cells of the pars intermedia. The sensitivity of the pituitary-adrenocortical system for the suppressive effect of dexamethasone was unaffected.
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PMID:Central diabetes insipidus in a dog with a pro-opiomelanocortin-producing pituitary tumor not causing hyperadrenocorticism. 853 Nov 85

Central diabetes insipidus is a chronic disorder which in most patients occurs secondary to tumor, infection, trauma or other lesions. In about 20-30% of patients etiology is unclear, however a destructive autoimmune process in the hypophysis may play a role. We report the case of an 18-year-old girl with central diabetes insipidus. Vasopressin levels were typically decreased. Examinations performed 1.5 years after manifestation showed no pathologic changes on MRI and no additional endocrine disorder. MRI was repeated 1.5 years later whereon a thickening of the pituitary stalk as a typical sign of hypophysitis was apparent. No other reasons could be found for the vasopressin deficiency. The finding of hypophysitis in our patient 3 years after disease manifestation suggests that the characteristic MRI changes may take as long as 3 years to become apparent.
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PMID:Diabetes insipidus due to hypophysitis. 903 Sep 72

Diabetes insipidus is an uncommon condition characterized by polyuria and polydipsia. The symptoms and biochemical changes of this condition result from either a lack of antidiuretic hormone or renal insensitivity to its effect. Failure to produce or release antidiuretic hormone may result from cranial pathology, including trauma and surgery. The renal insensitivity to antidiuretic hormone that occurs in patients with nephrogenic diabetes insipidus may be caused by genetic factors, drugs (especially lithium) or specific disease processes. Patients may compensate for polyuria and nocturia by excessive water intake but show marked decreases in urine specific gravity and osmolality. Patients with severe and uncompensated symptoms develop marked dehydration, neurologic symptoms and encephalopathy. The water deprivation test is useful in diagnosing diabetes insipidus and in differentiating neurogenic from nephrogenic cases. Neurogenic diabetes insipidus may respond to nasal administration of desmopressin. Nephrogenic diabetes insipidus requires good hydration and monitoring of body chemistry. Thiazides and amiloride may relieve symptoms.
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PMID:Evaluation and management of diabetes insipidus. 914 42

The paper describes a patient with Asperger disorder, Neurogenic Diabetes Insipidus (NDI) and Primary Empty Sella (ES). His response to vasopressin treatment suggested a concomitant presence of primary polydipsia. This is the first reported case of an autistic spectrum disorder associated with NDI or ES. The implications of the observed co-occurrence of these relatively rare disorders are discussed in relation to diagnosis and pathogenesis.
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PMID:Diabetes insipidus and polydipsia in a patient with Asperger's disorder and an empty sella: a case report. 965 35

Vasopressin, released from the posterior pituitary and from the vascular endothelium, can cause vasoconstriction and provoke platelet aggregation, leading to an impaired tissue blood supply. In humans with pituitary diabetes insipidus the central release of vasopressin is diminished, and in the Brattleboro homozygous rat there is congenitally no synthesis of this hormone. The gastroduodenal intramucosal vasopressin level is elevated in normal rats following various acute ulcerogenic challenges (after ethanol, reserpine, indomethacin, cold-restraint stress, endotoxin shock and hemorrhagic shock), and vasopressin-deficient rats are less sensitive to these stimuli. In a hospital- and population-based case-control, age-matched retrospective study, the incidence of human gastroduodenal ulceration is significantly higher in the normal population (in whom the release of vasopressin is presumed to be intact) than in the vasopressin-deficient one (central diabetes insipidus patients). In conclusion, endogenous vasopressin plays an aggressive role in development of gastroduodenal ulceration, especially that related to stress.
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PMID:Deleterious action of vasopressin in gastroduodenal ulceration: experimental and clinical observations. 986 15

Central diabetes insipidus (DI) is a rare complication of Wegener's granulomatosis (WG), which usually presents after pulmonary or kidney involvement. Anterior pituitary dysfunction secondary to WG has been extremely rare, documented in only three cases. We report a case of a 47-year-old postmenopausal woman who was diagnosed with hypopituitarism in November 1999 and started on vasopressin, thyroxine, and hydrocortisone. She sought treatment at the Mayo Clinic in February 2000 with a purpuric rash, fever, cough, shortness of breath, and blood in the sputum. Computed tomography of the chest showed a 6-cm irregular mass in the right lower lobe, and a biopsy of the mass showed marked reactive atypia and necrosis. Positive C-antineutrophil cytoplasmic antibodies (ANCA) and skin biopsy of a purpuric lesion showing leukocytoclastic vasculitis confirmed the diagnosis of WG. Hormonal studies showed low gonadotropins, thyroid-stimulating hormone (TSH), and prolactin. Magnetic resonance imaging (MRI) of the head showed cystic enlargement of the pituitary gland that did not enhance with gadolinium. Two months into the treatment with cyclophosphamide and prednisone, she had persistent pituitary dysfunction, despite the normal appearance of the pituitary gland on repeat MRI. We conclude that WG should be included in the differential diagnosis of DI and anterior pituitary dysfunction in the proper clinical setting. Early diagnosis and treatment may be crucial in preventing pituitary gland destruction and long-term endocrine sequelae. We suggest screening for anterior pituitary failure in the presence of the WG-associated DI.
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PMID:Diabetes insipidus and anterior pituitary insufficiency as presenting features of Wegener's granulomatosis. 1113 94

Central diabetes insipidus is clinically masked in dialysis patients. We report a 12-year-old girl receiving a living-related donor graft for renal failure from Alport syndrome, in whom a craniopharyngioma had been resected 6 months before transplantation. Pretransplant evaluation had documented central hypothyroidism, growth hormone deficiency, and presumptive hypogonadotropic hypogonadism. The corticotropin-releasing factor test had been normal. Four hours after transplantation, urine output exceeded 1,000 ml/h without diuretic therapy. Serum sodium concentration was 155 mmol/l, serum osmolality 333 mmol/kg, and plasma antidiuretic hormone 4.9 ng/l, while urine osmolality was 233 mmol/kg. Desmopressin acetate was started by continuous intravenous infusion at 1 microgram/day. Serum electrolytes rapidly normalized, urine output stabilized at 2 l/day. The patient was discharged 4 weeks after transplantation with good allograft function, receiving intranasal desmopressin acetate 10 micrograms twice daily. Pre-existing central diabetes insipidus is unmasked after successful kidney transplantation, leading to rapid dehydration and hypernatremia, which can be prevented by prompt institution of desmopressin therapy.
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PMID:Perioperative management of central diabetes insipidus in kidney transplantation. 1135 73


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